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Phase 2a > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Definition of osteoarthritis?

Why is not called “wear and tear” anymore?

A

Degenerative disease of joints resulintg in loss of articular cartilage

More complex - remodelling of bone and inflammation occurs

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2
Q

5 X-ray points of OA?

A 
Narrowed joint space
Osteophyte formation
Sub-chondral sclerosis
Sub-condral cysts
Abnormalities of bone contour
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3
Q

5 risk factors of osteoarthritis?
What cell will these risk factors affect?
What do they start producing instead?

A

Age, Biological sex, Obesity, Trauma, Sport

Chondrocyte activity

Produce type 1 collagen instead of type 2 collagen - will eventually undergo apoptosis

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4
Q 
PRESENTATION OF OA?
Hand nodes are called?
Limited ...?
Touch and it is...?
Would hear...?
Joint may be swollen because of...? (3)
A

Bouchard’s (PIP)
Heberden’s (DIP)

Limited range of movement

Tender

Crepitus

Bony enlargements, effusion, synovitis

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5
Q

What joints are commonly affect by OA:
In the hand?
3 others?

A

DIP (unique), PIP, 1st CMC

Knees, Hips, Lower lumbar spine

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6
Q

OA vs RA presentation:
Time?
Exercise? - why?
Symmetry?

A

OA: longer than 1 hour
RA: less than 30 minutes

OA: made worse with exercise (rubbing)
RA: made better with exercise (debris cleared)

OA: often non-symmetrical
RA: often symmetrical

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7
Q

What causes locking in OA?

What is name of the procedure for fixing it?

A

A loose body - bone or cartilage fragment

Removed with arthroscopy

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8
Q

3 categories of management in OA?

Examples in each…

A

Non-medical:
Patient education, activity & exercise, weight loss, physiotherapy, footwear, walking aids

Pharmacological:
Topical - NSAIDs, Capsaicin, Oral - Paracetamol, NSAIDs, Opioids,

Surgical:
Arthroscopy (loose bodies)
Osteotomy (change bone length)
Arthroplasty (replacements)

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9
Q

What is the classical population for RA?

What is the associated genetic link?

A

Middle-aged women (2 to 3 more times likely in women)

Association with HLA-DR4 (especially) and HLA-DR1

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10
Q

Presentation of RA:
What joints are normally affected? - common (4) and less common (4)

What other geneal symptoms might present? (4)

A

PIP, wrists, MTP, MCP
ankles, knees, elbows

Fever, malaise, myalgias, weight loss

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11
Q

RA on XRAY? (3)

A

Bony erosions
Soft tissue swelling
Narrowing of the joint space

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12
Q 
Extra-articular manifestations in RA:
Skin - 2
Vascular - 1
Eyes - 2
Pulmonary - 2
Lymph nodes become...?
Cyst name?
A

Skin: Raynaud’s, Nodules

Vascular: vasculitis

Eyes: scleritis, episcleritis

Pulmonary: pleural effusion, pulmonary fibrosis

Lymph nodes may become palpable

Baker’s Cyst

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13
Q

2 antibodies tested for in RA?
- percentage and explanation for one of these?
2 common complications of RA?

A

Rheumatoid Factor - IgM autoantibody against Fc poriton of IgG, 80% of case

Anti-CCP (anti-cyclic citrullinated peptide)

Anaemia of chronic disease - hepciin production
Secondary amyloidosis

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14
Q

What is Felty Syndrome?

High risk of…?

A

Rheumatoid Arthritis combined with…
Splenomegaly
Granulocytopenia/anaemia/neutropenia

High risk of infections

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15
Q

2 categories of management in RA:
2 examples -

4 examples -
B-cell one (CD20)
T-cell one
Three TNF ones

A

Disease-modifying anti-rheumatic medications (DMARDs):
Methotrexate & folic acid
Sulfasalazine

Biologics:
Rituximab (B-cells)
Abatacept (T-cells), Adalimumab, Etanercept, Infliximab (chemokines - TNF)

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16
Q

What are the two medications for acute flare-ups of RA?

A

NSAIDs and glucocorticoids

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17
Q

Crystal arthritis on microscopy:
Gout = ?
Pseudogout = ?

A

Monosoidum urate (negatively birefringent needles) = gout

Calcium pyrophosphate (weakly positive rhomboids) = pseudogout

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18
Q

What is urate crystals made from? 4 examples of these

Key enzyme involved in the metabolism of purines?

Main example of a known diseease that increase production of uric acid?

A

PURINES
Caffeine, xanthine, adenine, guanine

Xanthine oxidase

Lesch-Nyhan syndrome

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19
Q

What is major symptom in gout?
Main joint - special name? Why?
Other joints?

Chronic gout leads to:
“onion like aggregates” called…
increased risk of…

A

Severe pain and inflamed joint

Big toe (podagra)
Ankle/foot, knee, elbow, wrist

Tophi (aggregates of urate crystals)
Increased risk of kidney stones and urate nephropathy

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20
Q

What are the dietary triggers of gout?
Two non-dietary triggers?
Classic medication trigger?

A

Shellfish, red meat
Fructose, alcohol

MI, sepsis

Diuretics

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21
Q

GOUT MANAGEMENT:
Patient education = ?
Anti-inflammatory drugs = (3) and order
Specific drug? When is it used?

A

Patient education - hydration, diet, stay active

1st NSAIDs,
2nd colchicine,
3rd steroids

Recurring/chronic gout: xanthine oxidase inhibitor (allopurinol)

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22
Q

What is the name of the crystals in pseudogout?
Which joints to these typically affect?
Normal age of affected?

A

Calcium pyrophosphate

Typically knees and wrists

Elderly - often alongside degenerative disease

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23
Q

Osteoporosis definition vs Osteomalacia definition?

A

Osteoporosis - low bone mass and microarchitectural deterioration

Osteomalacia - softening of bone due demineralisation

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24
Q

Who does osteoporosis affect the most?
Primary risk factors for osteoporosis?
Secondary risk factors - diseases (two categories)

A

Elderly women - 1 in 3
1 in 5 men

Age, Menopause (oestrogen), genetics, smoking, low BMI, immobility

Chronic disease - inflammation causes resorption
Endocrine disease - parathyroid, thyroid, cortisol, oestrogen

25
Q

At what age do you have peak bone mass?
Overall principle of osteoporosis pathophysiology?
Two types?

A

Age 29 - possibly later in females?
RESORPTION > FORMATION
Post-menopausal (oestrogen effect)
Senile (osteoblasts worn out)

26
Q

What are the usual fractures that occur in osteoporosis? (3)

What is the name of the questionnaire used to predict risk?

A

Vertebral fractures - lumbar spine
Hip and wrist fractures

FRAX - predicts risk for those over 40

27
Q

What is the scan used to assess osteoporosis?
Produces a “..-score”

3 ranges and associated classification

A 
DEXA scan (dual X-ray absorptiometry scan)
T-score

Normal > -1
Osteopenia -1 to -2.5
Osteoporosis < 2.5

28
Q

Management of osteoporosis:
Lifestyle advice = ?
Anti-resorptive drugs - work by? Examples?
Anabolic - work by? Main example?

A

Education, stop smoking and alcohol, exercise, calcium and vitamin D diet

Anti-resorptive (decrease osteoclast activity)
• Bisphosphonates - 1st line, usually alendronate (disables osteoclasts)
• Denosumab - monoclonal antibody to RANK-L
• HRT - does increase other risks

Anabolic (increase osteoblast activity)
• Teriparatide (PTH analogue)

29
Q

What is the genetic association with spondyloarthritis?
What skeleton does it classically affect?
3 main examples
3 smaller examples

A

HLA-B27

Usually affect the AXIAL SKELETON

  • Ankylosing spondylitis
  • Reactive Arthritis (& Reiter’s syndrome)
  • Psoriatic arthritis

Enteropathic arthritis, Undifferentiated spondyloarthritis, Childhood arthritis

30
Q

What area of the world is AS classically common in?
Classic population?
UK prevalence?

A

High in Scandinavia - young adult males

0.5% prevalence in UK

31
Q

What joints does AS affect?
Leads to what presenting complaint?
What are the two classic associations?

A

Sacroiliac joint and spine (fusion - bamboo spine)

Lower back pain

Uveitis & Aortitis

32
Q

What is classic pathogen which causes Reactive arthritis? Other pathogen cateogry?
What is the two associations? - saying
Which joint?

A

Chlamydia trachomatis
Or general GI infection

arthritis, urethritis (circinate balanitis) and bilateral conjunctivitis - “can’t see, can’t pee, can’t climb a tree”

Monoarthritis of the knee

33
Q

How many cases of psoriasis have psoriatic arthritis?
Involves what joints? Specific joint causes what specific condition in fingers?
What nail changes can occur?

A

10% of cases

Involves axial and peripheral joints

Affects DIP - leading to dactylitis (sausage fingers and toes)
And psoriatic nail changes - pitting, onycholysis, hyperkeatosis

34
Q

What are the two categories of septic arthritis causes? How does each spread? How many or which joint in each?

A

N gonorrhoeae - spreads haematogenous, affects multiple joints, causes multiple lesions

NON-GONOCOCCAL ARTHRITIS: Often S aureus, affect single joint - often knee

35
Q

How does septic arthritis present?

What is the major risk in septic arthritis?

A

Joint - inflamed, with reduced ROM
Fever, increased WBC and elevated ESR

RISK: Intra-articular pressure compresses blood vessels and leads to necrosis

36
Q 
Osteomyelitis bacteria:
Two most common?
Salmonella is linked to?
Pasteurella is linked to?
Pseudomonas is linked to?
TB is called "... disease"
A

S aureus (most) & N gonorrhoeae

Salmonella (sickle cell)

Pseudomonas (diabetes or IV)

Pasteurella (dog/cat bite/scratch)

TB (Pott’s disease)

37
Q

Where does osteomyelitis normally affect in children and in adults?
What is a major risk factor for osteomyelitis?

A

Childen - metaphysis of long bones (mostly affects)
Adults - vertebrae

Prosthetic joints

38
Q

What are 3 types of osteomyelitis (spread)? Which population is affected by each?

A

Direct inoculation - those with recent trauma/surgery

Contingous spread - older adults

Haematogenous - children

39
Q

Name the two main inherited connective tissue disorders.

Name the four main autoimmune connective tissue disorders.

A

Marfan’s Syndrome
Ehler’s Danlos Syndrome

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)

SYSTEMIC SCLEROSIS (including CREST)

PRIMARY SJOGREN’S SYNDROME

DERMATOMYOSITIS/POLYMYOSITIS

40
Q

What would someone with Marfan’s look like?
What are the two major parts of the body that are affected by complications?
It is a mutation in what gene? What type of genetic disorder?

A

Tall, slender with long fingers

Lens dislocation in eyes
Aortic dilation, aneurysm and rupture

Mutation in FBN1 gene - Fibrillin 1 (autosomal dominant)

41
Q

The Ehler’s Danlos disorders cause a defect in what metabolism?
Mutations in what genes?

A

Collagen metabolism

COL5A or COL3A

42
Q

What is classic population affected by SLE?
Why this population specifically?
What another common trigger?
What type of hypersensitvity reaction?

A

Women of reproductive age
Link with non-white populations

Association with oestrogen

Medications

T3 hypersensitivty - immune complexes that cause inflammation

43
Q 
Presentation of SLE:
General - 3
Mucosa - 2
Skin - 3
Neurological - 2
Pulmonary - 1 + 2
Cardiovascular - 1 + 3
Renal - 1
Haematological - 3
Joints - 1
A

General - fever, malaise, weight loss

Mucosa - mouth/nose ulcers

Skin - UV sensitivity butterfly rash, photosensitive discoid rash, Raynaud’s

Neurological - headache, seizures

Pulmonary - pleuritis, pleural effusion, fibrosis

Cardiovascular - pericarditis, myocarditis, endocarditis (Libman-Sacks), HTN

Renal - nephritis

Haematological - anaemia, leukopenia, thrombocytopenia

Joints - arthritis (two or more)

44
Q

What is the biochemical test associated with SLE? Is it a good test?
What are the two major complications of SLE?

A

ANTINUCLEAR ANTIBODY (ANA) - sensitive, but not specific (RA, CREST, Sjogren’s)

Complications
Osteoporosis - low vitamin D (sun exposure)
Secondary antiphospholipid syndrome - hypercoagulable state due to antibody targeting proteins bound to phospholipid

45
Q

Systemic sclerosis:
Possible pathophysiology?
What does CREST stand for?

A

Unknown pathophysiology - possibly increased T-helper cells in skin

CREST - less severe form
Calcinosis - calcium deposition in skin
Raynaud’s - artery spasm in fingers
Oesophageal dysmotility - swallowing difficulty
Sclerodactyly - skin tightening over fingers
Telangiectasias - small dilated blood vessels on skin surface

46
Q

What are the two glands normally affected in Sjogren’s syndrome? What happens to them?
Other areas that can become affected?
Is it ANA positive?

A

Lacrimal glands: dry eyes (keratoconjunctivitis), eye problems
Salivary glands: xerostomia (cracks, fissures, taste/swallowing problems)

Can also affect nose, throat, skin, vagina

It is ANA-positive, specifically Anti-ssA and Anti-ssB

47
Q

What is the difference between polymyositis and dermatomyositis?

A

Polymyositis - multiple muscles - often shoulders, hips, thighs

Dermatomyositis - polymyositis with a skin rash (eyes, face, hands/fingers)

48
Q

What are the 3 main risk factors for bone malignancy?

A

Radiation - XR or CT
Paget’s disease
Familial retinoblastoma (osteosarcoma)

49
Q

What are the 5 cancers which often spread to bone?
Are these secondary tumours more or less common than primary tumours of bone?
Are they normally osteolytic or osteoblastic?
What is the exception to this?

A

Breast, prostate, kidney, thyroid, lung

More common than primary tumours

Usually osteolytic (punched-out) lesions

Apart from prostatic carcinoma - which classically produces osteoblastic lesions

50
Q

Name 4 out of the 5 benign tumours of bone?

A 
Osteoma
Osteoid osteoma
Osteoblastoma
Osteochondroma
Chondroma
51
Q

Name 3 malignant bone tumours

Where does each classically grow? (which bone and where in the bone?)

A

Osteosarcoma (osteoblasts) - (metaphysis, bones around knee)
Ewing sarcoma (neuroectoderm) - (diaphysis of long bones)
Chondrosarcoma (cartilage) - (medulla of pelvis or central skeleton)

52
Q

What is the classical population that suffers from fibromyalgia?
What actually is fibromyalgia?
Known pathophysiology?
Associations?

A

Muscle pain with no signs of inflammation

Non-specific muscular disorder with unknown cause (link to pain pathway problems)

10x more common in females, middle age, low household income, divorce

Associations: IBS, chronic headache, depression, chronic fatigue syndrome

53
Q

How does fibromyalgia present?
How long should it be present for?
How can you diagnose this?

A

Muscle pain worse with stress, cold, weather activity
Morning stiffness < 1 hour
Sleep disturbance (other symptoms)

Widespread symptoms of > 3 months

Presence of pain at specific palpation sites, suitable history, and associations present

54
Q

What is the difference between rickets and osteomalacia?
What links them together as a definition?
Pathophysiological princple?

A

Rickets - in children (softening, impaired growth, malformations)
Osteomalacia - in adults (weakening, softening)

“bone softening - faulty process of bone mineralisation”

Impaired vitamin D, phosphate or calcium metabolism
Therefore, reduced mineralization

55
Q

What are the risk factors for developing osteomalacia/rickets? (4)

A 
VIT D DEFICIANT: 
Malabsorption (coeliac or Crohn's), 
Reduced UV light, 
Medications - anticonvulsants, 
Liver and Kidney disease
56
Q

How does someone with osteomalacia present? (5)

A 
Diffuse bone and joint pain
Proximal muscle weakness
Bone fragility
Increased risk of fractures
Muscle spasms and numbness
57
Q

How does a child with Ricket’s present? (5)

A 
Craniotabes (softening or thinning of the skull)
Delayed closure of fontanelles
Genu varum (varus, bow-legs)
Protruding abdomen
Prominent frontal bone
58
Q

What is the proper name for “brittle bone disease”
What is the most severe type?
What happens to the eyes?

A

Osteogenesis imperfecta - type 1 collagen is affected
Type I is mild, Type II is severe
Association with blue sclerae

59
Q

What occurs in Paget’s disease of bone? (basic pathophysiology)
Early on it is…
Over time (3)

A

Excessive bone resorption followed by excessive bone grwoth after osteoclast burn out

Early on it is asymptomatic

Over time:
Can impinge on nerves (pain)
Overgrowth - leontiasis (caveman face), hearing loss, vision loss
Risk of osteosarcoma

Phase 2a (9 decks)

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